Figure 6. Areg promotes human intestinal myofibroblast proliferation and motility through activation of mTOR and MEK.

(A) Intestinal MFs isolated from CD patients were treated with or without 100 ng/ml Areg for 48h, and Ki67⁺ cells were analyzed by immunofluorescence. (B) Human intestinal MFs were wounded and treated with the 100 ng/ml Areg. Images were recorded with Biotek Cytation 5. (C) Human intestinal MFs were treated with or without the 100 ng/ml Areg in the presence or absence of Rapamycin or U0126 for 48h, and Col1a1 expression was determined by qRT-PCR. (D) Intestinal MFs were treated with Areg for 48h, and phosphorylation of mTOR and MEK was determined by western blot. (E) Human intestinal MFs were treated with or without 100 ng/ml Areg in the presence or absence of Rapamycin (mTOR inhibitor) or U0126 (MEK inhibitor) for 48h, and Ki67⁺ cells were analyzed by immunofluorescence. (F) Human intestinal MFs were wounded and treated with or without the 100 ng/ml Areg in the presence or absence of Rapamycin or U0126, and images were recorded by Biotek Cytation 5. Representative data from 2–3 independent experiments with similar results. (A-B, and D) Unpaired Student’s t-test; (C, and E-F) one-way ANOVA. *p < .05; **p < .01; ***p < .001; ****p < .0001.